Exact Mass: 496.2757676
Exact Mass Matches: 496.2757676
Found 42 metabolites which its exact mass value is equals to given mass value 496.2757676,
within given mass tolerance error 3.2E-7 dalton. Try search metabolite list with more accurate mass tolerance error
6.4E-8 dalton.
APGPR Enterostatin
Enterostatin APGPR (Ala-Pro-Gly-Pro-Arg) is a pentapeptide released from procolipase during fat digestion. In addition to the pancreas, enterostatin-immunoreactive cells are also present in the antrum and proximal small intestine. Enterostatin selectively reduces fat intake, decreases insulin secretion, and also increases energy expenditure by activating brown adipose tissue during high-fat feeding. Enterostatins are pentapeptides derived from the NH2-terminus of procolipase after tryptic cleavage and belong to the family of gut-brain peptides. Enterostatin is generated by the action of trypsin on procolipase in the intestinal lumen. Its structure is highly conserved in evolution, with an amino acid sequence of XPXPR. Three enterostatin sequences, Val-Pro-Asp-Pro-Arg (VPDPR), Val-Pro-Gly-Pro-Arg (VPGPR), and Ala-Pro-Gly-Pro-Arg (APGPR), have been studied extensively and shown to be almost equally effective in their ability to decrease dietary fat preference. Enterostatins are selective inhibitors of appetite, particularly of fat intake. Hyperenterostatinemia in obesity is probably secondary to enterostatin resistance; therefore, the regulatory system is producing more enterostatin to counteract the resistance. This is very similar to hyperinsulinemia and hyperleptinemia in obesity. The diminution in the meal-induced secretion of enterostatin in obesity suggests a delay in the appearance of satiety, leading to increased caloric intake. In rats enterostatin decreases body weight by decreasing fat-calorie intake and increasing the sympathetic firing rate of the nerves in interscapular brown adipose tissue. Enterostatin levels are elevated in the plasma of obese women, and enterostatin secretion is diminished after satiety. Oral administration of enterostatin, however, has no effect on food intake, energy expenditure, or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance, and the physiology of enterostatin in humans remains to be defined. (PMID: 10084574, 9526102, 8886249) [HMDB] Enterostatin APGPR (Ala-Pro-Gly-Pro-Arg) is a pentapeptide released from procolipase during fat digestion. In addition to the pancreas, enterostatin-immunoreactive cells are also present in the antrum and proximal small intestine. Enterostatin selectively reduces fat intake, decreases insulin secretion, and also increases energy expenditure by activating brown adipose tissue during high-fat feeding. Enterostatins are pentapeptides derived from the NH2-terminus of procolipase after tryptic cleavage and belong to the family of gut-brain peptides. Enterostatin is generated by the action of trypsin on procolipase in the intestinal lumen. Its structure is highly conserved in evolution, with an amino acid sequence of XPXPR. Three enterostatin sequences, Val-Pro-Asp-Pro-Arg (VPDPR), Val-Pro-Gly-Pro-Arg (VPGPR), and Ala-Pro-Gly-Pro-Arg (APGPR), have been studied extensively and shown to be almost equally effective in their ability to decrease dietary fat preference. Enterostatins are selective inhibitors of appetite, particularly of fat intake. Hyperenterostatinemia in obesity is probably secondary to enterostatin resistance; therefore, the regulatory system is producing more enterostatin to counteract the resistance. This is very similar to hyperinsulinemia and hyperleptinemia in obesity. The diminution in the meal-induced secretion of enterostatin in obesity suggests a delay in the appearance of satiety, leading to increased caloric intake. In rats enterostatin decreases body weight by decreasing fat-calorie intake and increasing the sympathetic firing rate of the nerves in interscapular brown adipose tissue. Enterostatin levels are elevated in the plasma of obese women, and enterostatin secretion is diminished after satiety. Oral administration of enterostatin, however, has no effect on food intake, energy expenditure, or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance, and the physiology of enterostatin in humans remains to be defined. (PMID: 10084574, 9526102, 8886249). Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake. Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake.
His Lys Asn Val
His Lys Val Asn
His Asn Lys Val
His Asn Val Lys
His Val Lys Asn
His Val Asn Lys
Lys His Asn Val
Lys His Val Asn
Lys Asn His Val
Lys Asn Val His
Lys Val His Asn
Lys Val Asn His
Asn His Lys Val
Asn His Val Lys
Asn Lys His Val
Asn Lys Val His
Asn Val His Lys
Asn Val Lys His
Pro Pro Gln Arg
Pro Pro Arg Gln
Pro Gln Pro Arg
Pro Gln Arg Pro
Pro Arg Pro Gln
Pro Arg Gln Pro
Gln Pro Pro Arg
Gln Pro Arg Pro
Gln Arg Pro Pro
Arg Pro Pro Gln
Arg Pro Gln Pro
Arg Gln Pro Pro
Val His Lys Asn
Val His Asn Lys
Val Lys His Asn
Val Lys Asn His
Val Asn His Lys
Val Asn Lys His
APGPR
Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake. Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake.
APGPR Enterostatin
Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake. Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake.